AT 1 Blockade Prevents Glucose-Induced Cardiac Dysfunction in Ventricular Myocytes
Why the study?
Does AT1 blockade prevent high glucose-induced cardiac contractile dysfunction in rat ventricular myocytes?
Population
Rat ventricular myocytes maintained in normal- or high- glucose medium for 24 hours
Comparison
AT1 blocker L-158,809 (10 to 1000 nmol/L) vs High glucose medium without AT1 blocker, or JAK2…
Design
Preclinical
Follow-up
24 hours
Authors
Discussion
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Implication
Implicates AT1 signaling in rat myocyte glucose toxicity; hypothesis-generating, should not yet change practice.
Structured PICO
Does AT1 blockade prevent high glucose-induced cardiac contractile dysfunction in rat ventricular myocytes?
P
Population
Rat ventricular myocytes maintained in normal- (NG, 5.5 mmol/L) or high- (HG, 25.5 mmol/L) glucose medium for 24 hours
I
Intervention
AT1 blocker L-158,809 (10 to 1000 nmol/L)
C
Comparator
High glucose medium without AT1 blocker, or JAK2 inhibitor AG-490 (10 to 100 micromol/L)
O
Outcome
Mechanical and intracellular Ca2+ properties (peak shortening, time to PS, time to 90% relengthening, maximal velocity of shortening/relengthening, and intracellular Ca2+ decay)surrogate
Local Ang II, acting via AT1 receptor-mediated NADPH oxidase activation, is involved in hyperglycemia-induced cardiomyocyte dysfunction, which can be prevented by AT1 blockade.
Cite This Study
Privratsky et al. (2003) studied this question.